Stabilization of β-catenin impacts pancreas growth

A recent study has shown that deletion of β-catenin within the pancreatic epithelium results in a loss of pancreas mass. Here, we show that ectopic stabilization of β-catenin within mouse pancreatic epithelium can have divergent effects on both organ formation and growth. Robust stabilization of β-catenin during early organogenesis drives changes in hedgehog and Fgf10 signaling and induces a loss of Pdx1 expression in early pancreatic progenitor cells. Together, these perturbations in early pancreatic specification culminate in a severe reduction of pancreas mass and postnatal lethality. By contrast, inducing the stabilized form of β-catenin at a later time point in pancreas development causes enhanced proliferation that results in a dramatic increase in pancreas organ size. Taken together, these data suggest a previously unappreciated temporal/spatial role for β-catenin signaling in the regulation of pancreas organ growth.